Nucleotide metabolism: secondary hyperuricaemia in psoriasis: practice question

A Biochemistry question in the style of the NEET PG paper. Answer it first, then read why the right option is right and why each of the others is wrong.

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Biochemistry · Nucleotide metabolism: secondary hyperuricaemia in psoriasis

Sample item

A man with extensive psoriasis, normal renal function and no medication has a serum urate of 9 mg/dL. Which mechanism most likely explains this?

ADeficient xanthine oxidase blocking the last step of purine degradationBRapid cell turnover increasing nucleic acid breakdown to uric acidCAbsence of uricase in all humans, causing the raised urateDHGPRT deficiency raising PRPP and de novo purine synthesis

Original practice item, not a recalled exam question. Nothing here is recorded.

The answer and the reasoning

B. Rapid cell turnover increasing nucleic acid breakdown to uric acid

Conditions with accelerated cell turnover, including psoriasis, leukaemia and haemolysis, increase nucleic acid catabolism, so more purine is converted to uric acid. Lack of uricase is universal in humans, so it cannot explain a raised level in one person.

Option by option

A. Deficient xanthine oxidase blocking the last step of purine degradation
Xanthine oxidase deficiency would lower urate rather than raise it.
B. Rapid cell turnover increasing nucleic acid breakdown to uric acid (correct)
Correct. High epidermal cell turnover releases more purines for degradation.
C. Absence of uricase in all humans, causing the raised urate
All humans lack uricase, so this is not why this patient differs from others.
D. HGPRT deficiency raising PRPP and de novo purine synthesis
HGPRT deficiency is a rare X-linked disorder with neurological features, not an explanation in a skin disease.

Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.

Questions about this Biochemistry question

What is the answer to this Biochemistry question?

The best answer is B, Rapid cell turnover increasing nucleic acid breakdown to uric acid. Conditions with accelerated cell turnover, including psoriasis, leukaemia and haemolysis, increase nucleic acid catabolism, so more purine is converted to uric acid.

Why is "Deficient xanthine oxidase blocking the last step of purine degradati…" not the answer?

Xanthine oxidase deficiency would lower urate rather than raise it.

Why is "Absence of uricase in all humans, causing the raised urate" not the answer?

All humans lack uricase, so this is not why this patient differs from others.

Why is "HGPRT deficiency raising PRPP and de novo purine synthesis" not the answer?

HGPRT deficiency is a rare X-linked disorder with neurological features, not an explanation in a skin disease.

What concept does this question test?

It tests Nucleotide metabolism: secondary hyperuricaemia in psoriasis in Biochemistry. Lack of uricase is universal in humans, so it cannot explain a raised level in one person.

How hard is this question?

We tag it as an application question: it asks you to use a fact on a patient or a finding. The tag is our own editorial judgement, not an official difficulty rating, so read the reason for every option, not only the answer.

How should I study Nucleotide metabolism: secondary hyperuricaemia in psoriasis?

Build one table of enzyme deficiency, disease, inheritance and key finding, then revise it by spaced recall. Then use the flashcards and the other Biochemistry questions on this site to test what stuck.

Is this a real NEET PG question?

No. It is an original practice item (editorial status: sample, version 1). NextPrep does not publish recalled or leaked questions, and independent faculty review of this item has not been completed yet, so confirm important facts in a standard textbook.